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A 77-year-old woman was admitted due to AV graft thrombosis; given the technical impossibility of performing other native AV fistulas, we chose to insert a tunnelled central venous catheter. Considering the vascular history of the patient, the central venous catheter could not be placed into the internal jugular vein; it was therefore put into the left femoral vein. Following a 3-month-period of the catheter working properly, the patient was hospitalized due to sudden acute pain in the left thigh. In a few days the patient developed an important haematoma with serious anemization in the left lower limb. Ultrasonography showed the presence of a fistula between the left common femoral artery and the femoral vein, leading to the subsequent successful positioning of a stent into the common femoral artery through right trans-femoral access. Angiography examination showed the femoral vein patency along the proximal stretch with respect to the function of the tunnelled venous catheter.

Organic anion transporters (OATs), which are expressed in proximal tubule cells, mediate diuretic secretion into tubular fluid. Increased plasma levels of organic anions and urate and metabolic acidosis, i.e. two characteristic features of chronic renal insufficiency, could be factors contributing to diuretic resistance. These limitations demand increasing doses of diuretics up to a maximum level, or the use of a loop diuretic with non-renal metabolism. Diuretic responsiveness in nephrotic syndrome is limited by strong Na+ reabsorption in the distal nephron. Strategies to improve loop diuretic responsiveness include diuretic dosage and the combination of a loop diuretic with a distal acting diuretic. Strategies to limit protein excretion include the use of angiotensin converting enzyme inhibitors or angiotensin receptor blockers and appropriate salt intake limitation.

In absence of a permanent and useful native arterio-venous fistula, the use of a tunnelled catheter allows dialysis therapy to be carried out. The Ash Split Cath is a recently introduced chronic hemodialysis catheter. An ASC was inserted in nine patients (7.1% of our prevalent dialysis population), for repeated venous thrombosis in seven patients and a poor venous tree in two. The average blood flow rate was 250 +/- 50 mL/minute and the mean venous pressure measured was 140mm Hg +/- 35. Recirculation determined by low flow technique was less than 5% and 4 months after the catheter placement, calculated Kt/V, was 1.2 +/- 0.02. During the follow up we did not document any infection of the exit site or related to the catheter.

Pre-eclampsia is a pregnancy-specific disorder that presents major health problems for both mothers and babies. It is a major cause of maternal mortality, especially in developing countries, where it may account for 80% of maternal deaths. In this review we have discussed the putative pathogenetic mechanisms of this severe illness.Review of the international literature on pre-eclampsia.Pre-eclampsia occurs predominantly in primigravidas and is associated with increased foetal and maternal risk. Generally speaking, one could hypothesise that during pre-eclampsia the oxidative, coagulative and vasomotor balance is altered by increased sensitivity to angiotensin II associated with reduced synthesis of vasodilator prostaglandins, sympathetic nervous system hyperactivity, hyperlipidaemia associated with raised lipoperoxide synthesis and incomplete implant of cytotrophoblast in maternal spiral arteries. General vasoconstriction could then be a consequence with related utero-placental ischaemia and endothelial damage. These features are clinically characterised by arterial hypertension, proteinuria and sodium retention. The predisposition to develop pre-eclampsia seems to be at least partially hereditary and the risk seems to be transmissible through male sons. To explain the susceptibility of some women to develop pre-eclampsia, specific genetic polymorphisms have been associated to increased risk.Many factors are involved in the pathogenesis of pre-eclampsia. Occasionally these factors seem to act together, sometimes they do not and, consequently, it might be difficult to postulate a common pathogenesis for the disorder. Good obstetrical practice will identify known risk factors but will not enable physicians to determine the risk value for a particular pregnancy. Moreover, we are far from understanding the exact mechanisms involved, let alone acting upon them. The achievement of these objectives constitute a remarkable challenge for research.